Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patterns of breathing at night were recorded in 4 patients with heart-failure. 2 had periodic breathing while awake and in 2 it developed after they fell asleep. In all 4 the phase of hyperventilation disturbed sleep. These cases also illustrate other problems caused by periodic respiration in heart-failure, which range from tiredness during the day to an inability to sleep for more than a few minutes. Nocturnal waking in the hyperventilation phase of Cheyne-Stokes breathing should be differentiated from paroxysmal nocturnal dyspnoea caused by episodes of pulmonary oedema at night.
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PMID:Paroxysmal nocturnal dyspnoea and periodic respiration. 9 69

Five patients with congestive heart failure (CHF) and 1 with left ventricular dysfunction but without CHF were found to have sleep apnea. Central sleep apnea (CSA) related to Cheyne-Stokes respiration was seen in 4 cases while obstructive sleep apnea (OSA) was seen in 2. All patients had symptoms of sleep apnea. Nasal continuous positive airway pressure (NCPAP) was effective in reversing CSA and OSA in all patients with improvement in sleep structure and alleviation of symptoms of sleep apnea. In addition, all experienced a reduction in cardiac dyspnea. This was associated with a 5% or greater increase in left ventricular ejection fraction while on NCPAP, compared to baseline value off NCPAP in 5 patients and resolution of chronic pleural effusion and pulmonary edema in the sixth. We conclude that Cheyne-Stokes respiration during sleep may give rise to a CSA syndrome that is reversible by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function in patients with left ventricular dysfunction and sleep apnea.
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PMID:Sleep apnea in patients with left ventricular dysfunction: beneficial effects of nasal CPAP. 219 97

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

Due to its high prevalence in patients with heart failure and its negative predictive value concerning morbidity and mortality, Cheyne-Stokes respiration (CSR) is a sleep disorders of major interest. CSR correlates with the degree of heart failure and is characterised by a typical crescendo/decrescendo breathing pattern combined with phases of central sleep apnoea, caused by pulmonary oedema and oscillation of ventilatory control. Thus, CSR is a marker of the severity of heart failure. Treatment of CSR first involves optimisation of heart failure therapy by cardiologists and then application of non-invasive means of ventilatory support. Treatment of patients with severe heart failure with non-invasive positive pressure ventilatory support leads to a significant reduction of CSR, sympathetic activity, and daytime sleepiness and improves cardiac output and 6-minute walking distance. At present, a prospective randomised, controlled intervention-study (Serve-HF study) is being conducted in order to show if therapy of CSR can improve patient survival. This review describes the pathophysiology, epidemiology, and therapeutic options of CSR with a special focus on the elevated cardiovascular risk of patients with CSR.
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PMID:[Cheyne-Stokes respiration and cardiovascular risk]. 1959 Oct 86